作者: NICHOLAS SMIRNOFF
DOI: 10.1111/J.1469-8137.1993.TB03863.X
关键词: Antioxidant 、 Biochemistry 、 Oxidative stress 、 Superoxide dismutase 、 Chemistry 、 Photosynthesis 、 Photorespiration 、 Desiccation tolerance 、 Superoxide 、 Lipid peroxidation
摘要: SUMMARY Water deficits cause a reduction in the rate of photosynthesis. Exposure to mild water deficits, when relative content (RWC) remains above 70%, primarily causes limitation carbon dioxide uptake because stomatal closure. With greater direct inhibition photosynthesis occurs. In both cases fixation results exposure chloroplasts excess excitation energy. Much this can be dissipated by various photoprotective mechanisms. These include dissipation as heat via carotenoids, photorespiration, CAM idling and, some species, leaf movements and other morphological features which minimize light absorption. The active oxygen species superoxide singlet are produced photoreduction Oxygen energy transfer from triplet excited chlorophyll oxygen, respectively. Hydrogen peroxide hydroxyl radicals form result reactions superoxide. All these reactive potentially damaging, causing lipid peroxidation inactivation enzymes. They normally scavenged range antioxidants enzymes present chloroplast subcellular compartments. When is limited deficit, formation increases energy, not fay mechanisms, used oxygen. However, photorespiratory hydrogen production peroxisomes decreases. Increased detected EPR (electron paramagnetic resonance) droughted plants. Stiperoxide leads changes suggestive oxidative damage including decrease ascorbate. not, however, apparent until severe develop, they could also interpreted secondary effects deficit-induced senescence or wounding. Non-lethal often increased activity dismutase, glutathione reductase monodehydroascorbate reductase. capacity protective may part general antioxidative response plants involving regulation protein synthesis gene expression. Since treatments damage, alter balance between input such low temperature high irradiance, it suggested that deficit has same effect. Light levels excessive do become photoprotective/antioxidative systems activated. Some mechanisms themselves formation. Photoinhibitory includes component damage. During normally-encountered degrees antioxidant their ability respond generation sufficient prevent overt expression damage. Desiccation-tolerant tissues bryophytes, lichens, spores, seeds, algae few vascular plant leaves survive desiccation below 30–40% RWC, A seeds bacteria oxygen-dependent. Desiccation oxidation glutathione, major antioxidant, appearance free radical signal number suggesting occurred. photosynthetic cells arise photooxidation. Disruption membrane-bound electron tranport partially hydrated tissue lead Oxidation lipids sulphydryl groups occur dry tissue. Tolerant recover upon rehydration arc able reduce pool. Non-tolerant go on show further peroxidation. It difficult attribute subsequent effect death. Embryos lose tolerance soon after imbibition. This associated with membrane been attributed superoxide-mediated deesterification phospholipids loss lipophilic antioxidants. discussed relation involved tolerance.